Remote patient monitoring should reduce mortality rates, improve care, and reduce costs. We present an overview of the available technologies for the remote monitoring of chronic obstructive pulmonary disease (COPD) patients, together with the most important medical information regarding COPD in a language that is adapted for engineers. Our aim is to bridge the gap between the technical and medical worlds and to facilitate and motivate future research in the field. We also present a justification, motivation, and explanation of how to monitor the most important parameters for COPD patients, together with pointers for the challenges that remain. Additionally, we propose and justify the importance of electrocardiograms (ECGs) and the arterial carbon dioxide partial pressure (PaCO2) as two crucial physiological parameters that have not been used so far to any great extent in the monitoring of COPD patients. We cover four possibilities for the remote monitoring of COPD patients: continuous monitoring during normal daily activities for the prediction and early detection of exacerbations and life-threatening events, monitoring during the home treatment of mild exacerbations, monitoring oxygen therapy applications, and monitoring exercise. We also present and discuss the current approaches to decision support at remote locations and list the normal and pathological values/ranges for all the relevant physiological parameters. The paper concludes with our insights into the future developments and remaining challenges for improvements to continuous remote monitoring systems.
Graphical abstractᅟ
High on-treatment platelet reactivity (HTPR) on clopidogrel correlates with adverse outcomes in patients treated with percutaneous coronary intervention (PCI). Whether HTPR is a modifiable risk factor for future events is not clear. We evaluated the effect of serial clopidogrel dose adjustment based on platelet function testing (PFT) during 12 months of dual antiplatelet therapy (DAPT) using Multiplate) analyzer in patients with HTPR after PCI in acute coronary syndrome on clinical outcome. Eighty-seven patients were randomized to interventional (n = 43) and control group (n = 44). Blood samples for PFT were drawn at day 1, 2, 3, 7, 30 and at month 2, 3, 6, 9 and 12. Clopidogrel dose was modified at each point of PFT in the interventional group with patients taking up to two additional 600 mg loading doses and a range of 75-300 mg maintenance dose to achieve and maintain optimal platelet reactivity (19-46 U). The incidence of the primary endpoint (composite of cardiovascular death, non-fatal myocardial infarction, target vessel revascularization and ischemic stroke) was significantly higher in the control group (36.3 vs. 16.2%; p = 0.034). There were no differences in total bleeding events (6.8 vs. 4.6%, p = ns). Patients in the interventional group maintained better P2Y12 inhibition during follow-up. We hypothesize that targeting the therapeutic window of platelet reactivity continuously throughout DAPT by dose adjustment of P2Y12 inhibitor may lead to better platelet reactivity control, and thus reduce the rate of ischemic complications in this high risk group of patients.
Chronic heart failure places heavy burden on patients, their families and on health care resources, accounting for high numbers of hospital admissions. Despite huge improvements in the treatment of many heart disorders, the clinical syndrome of chronic heart failure as a final pathway of heart pathology is an exception, in that its prevalence is rising, and only small prolongations in survival are occurring. It is associated with high morbidity and poor prognosis, and a survival rate worse than that for some malignant tumors. The reasons for the increasing overall prevalence of chronic heart failure in developed countries lie in prolonged survival owing to modern pharmacological or invasive treatment, better secondary prevention, and aging of the population. Chronic pulmonary disease is common in patients with chronic heart failure. Through sharing some risk factors and overlapping pathophysiological processes, they present diagnostic and therapeutic challenge. The aim of this article is to review various mechanisms responsible for the symptoms of chronic heart failure with consecutive pulmonary interaction and abnormalities in lung function.
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